To validate Ullanlinna Narcolepsy Scale (UNS) as a screening tool for narcolepsy in a clinical population and to compare it with Swiss Narcolepsy Scale (SNS) and Epworth Sleepiness Scale (ESS). UNS questionnaires of 267 participants visiting Helsinki Sleep Clinic were analyzed. The diagnoses of the participants were narcolepsy type 1 (NT1, n = 89), narcolepsy type 2 (NT2, n = 10), other hypersomnias (n = 24), sleep apnea (n = 37), restless legs syndrome or periodic limb movement disorder (n = 56), and other sleep-related disorders (n = 51). In addition, ESS and SNS scores in a subset of sample (total N = 167) were analyzed and compared to UNS. Mean UNS score in NT1 was 22.0 (95% confidence interval [CI] = 20.4 to 23.6, range 9–43), which was significantly higher than in other disorders, including NT2 (mean 13.7, 95% CI = 10.3 to 17.1, range 7–21, p = .0013). Sensitivity and specificity of UNS in separating NT1 from other disorders were 83.5% and 84.1%, respectively. Positive and negative predictive values were 82.5% and 85.1%, respectively. Sensitivities of SNS and ESS in NT1 were 77.2% and 88.6%, and specificities 88.6% and 45.5%, respectively. There were no differences in receiver operating characteristic curves between UNS and SNS. UNS had moderate negative correlation with hypocretin-1 levels (rs = –.564, p < .001), and mean sleep latency in multiple sleep latency test (rs= –.608, p < .001). UNS has high specificity and sensitivity for NT1 in a sleep clinic setting. UNS scores below 9 strongly suggest against the diagnosis of narcolepsy.
A standardized questionnaire was mailed to all employees of the Finnish Broadcasting Company with irregular shift work (n = 750) and to an equal number of randomly selected controls in the same company with regular 8-hour daytime work. The aims were to investigate the prevalence and severity of perceived orofacial pain (Research Diagnostic Criteria for Temporomandibular Disorders Axis II) and to analyze whether current orofacial pain was associated with reported bruxism and insomnia symptoms (Diagnostic and Statistical Manual of Mental Disorders-IV and the International Classification of Sleep Disorders Revised). The response rate in the irregular shift-work group was 82.3% (56.6% men) and in the regular daytime-work group 34.3% (46.7% men). Current orofacial pain was found overall in 19.6%, of which 88.3% had experienced the pain over 6 months. All claimed that their pain fluctuated. No subjects with chronic orofacial pain reported disabling pain, and grades III and IV were not found. Insomnia symptoms and frequent bruxism were significantly more prevalent in chronic pain grade II than in lower grades. According to logistic regression, current orofacial pain was significantly positively associated with frequent bruxism (p < 0.001), female gender (p < 0.001), and disrupted sleep (p < 0.01), and significantly negatively associated with age over 45 years (p < 0.01). Our results revealed a clear-cut association between perceived orofacial pain and reported bruxism. The association held with both chronic orofacial pain intensity and current pain. Based on the multivariate analyses, it can be concluded that disrupted sleep and bruxism may be concomitantly involved in the development of orofacial pain.
Both gamma-aminobutyric acid (GABA)(C) receptor subunit mRNA and protein are expressed in the stratum pyramidale in the CA1 area of the adult rat hippocampus, but so far no conclusive evidence about functional hippocampal GABA(C) receptors has been presented. Here, the contribution of GABA(C) receptors to stimulus-evoked postsynaptic potentials was studied in the hippocampal CA1 area with extracellular and intracellular recordings at the age range of 21-47 postnatal days. Activation of GABA(C) receptors with the specific agonist cis-4-aminocrotonic acid (CACA) suppressed postsynaptic excitability and increased the membrane conductance. The GABA(C) receptor antagonist 1,2,5,6-tetrahydropyridine-4-ylmethylphosphinic acid (TPMPA), but not the GABA(A) receptor antagonist bicuculline, inhibited the effects of CACA. GABA-mediated long-lasting depolarizing responses evoked by high-frequency stimulation of local inhibitory interneurons in the CA1 area in the presence of ionotropic glutamate receptor and GABA(B) receptor blockers were prolonged by TPMPA, indicating that GABA(C) receptors are activated under these conditions. For weaker stimulation, the effect of TPMPA was enhanced after GABA uptake was inhibited. Our data demonstrate that GABA(C) receptors can be activated by endogenous synaptic transmitter release following strong stimulation or under conditions of reduced GABA uptake. The lack of GABA(C) receptor activation by less intensive stimulation under control conditions suggests that these receptors are extrasynaptic and activated via spillover of synaptically released GABA.
